SLC2A4 Antibody
- Known as:
- SLC2A4 Antibody
- Catalog number:
- abx000041
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- SLC2A4 Antibody
Related genes to: SLC2A4 Antibody
- Gene:
- SLC2A4 NIH gene
- Name:
- solute carrier family 2 member 4
- Previous symbol:
- GLUT4
- Synonyms:
- -
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-06
- Date modifiied:
- 2016-10-05
Related products to: SLC2A4 Antibody
Related articles to: SLC2A4 Antibody
- Mild thermal stimulation enhances skeletal muscle differentiation; however, its underlying metabolic basis remains unclear. Here, we demonstrate that thermal stimulation promotes myogenic differentiation through enhanced glucose uptake and transient lipid droplet (LD) accumulation in C2C12 myoblasts. Thermal stimulation at 39 °C induced a transient increase in LD formation during early differentiation. Early transient LD accumulation, particularly on days 1 and 2, was positively correlated with the day 5 fusion index, suggesting that early LD formation is associated with subsequent myogenic differentiation. Suppression of LD formation by Plin2 knockdown impaired myotube formation, indicating that LD formation is functionally required for myogenic differentiation. Thermal stimulation enhanced glucose uptake, accompanied by increased Slc2a4 and Ppargc1a expression and increased GLUT4 fluorescence intensity. Moreover, higher glucose availability further supported LD formation and myogenic differentiation even under serum-free conditions. Notably, mitochondrial mass, ATP content, and oxidative capacity remained largely unchanged, suggesting that enhanced glucose uptake is associated with LD accumulation without a corresponding increase in mitochondrial oxidative capacity. These findings identify transient LD formation as a key metabolic event driving myogenic differentiation under thermal stimulation. - Source: PubMed
Publication date: 2026/08/05
Mahzabin RumanaHayashi SatokoHabib Md RezwanulTokutake YukakoYonekura Shinichi - Euphorbia antiquorum L. (Euphorbiaceae), a traditionally used Asian medicinal plant, was systematically evaluated for its antidiabetic efficacy through a bioactivity-guided approach integrating in vitro, in vivo, and in silico studies. Among the four solvent fractions of the ethanolic stem extract, the ethyl acetate fraction exhibited the highest antioxidant and glucose utilization activity. Column chromatography of the ethyl acetate fraction yielded several subfractions, among which Fraction 2 (CEA2) showed strong antioxidant activity and significantly enhanced glucose utilization and GLUT4 translocation (p < 0.01). In a 63-day high-fat high-fructose diet and low-dose streptozotocin-induced diabetic rat model, CEA2 (200 and 400 mg/kg) markedly reduced fasting blood glucose, improved body weight, restored biochemical parameters, and decreased TNF-α and IL-6 levels, while also improving pancreatic and hepatic histopathology. Western blotting confirmed significant upregulation of plasma membrane GLUT4 (p < 0.01). LC-MS profiling identified major compounds, including 3-O-trans-p-coumaroyltormentic acid and geranyl acetoacetate, which demonstrated strong binding to IRS-1 and Akt-PKB in docking and molecular dynamics analyses, key regulators of GLUT4 vesicle mobilization. This study provides one of the first comprehensive validations establishing CEA2 as a potent modulator of insulin signaling and GLUT4 mobilization, supporting E. antiquorum as a promising phytopharmaceutical candidate for type 2 diabetes management. - Source: PubMed
Saikia LunasmritaDutta Partha PratimGogoi DhurbajyotiAfzal Nazim UnddinManna PrasenjitLaw DouglasMandal SantaGogoi BhaskarjyotiGautam Manish KumarSen Saikat - Obesity induced by high‑fat, high‑sucrose diets (HFSD) remains a major global health challenge, disrupting lipid metabolism, glucose homeostasis, and gut microbial balance. These disturbances underscore the need for safe interventions capable of restoring metabolic regulation. Senna alexandrina (SA), traditionally used for weight reduction, has recently been shown to modulate the gut microbiota beyond its laxative effects. To enhance efficacy while minimizing adverse outcomes, this study investigated the effects of a low and safe dose of SA combined with intermittent fasting (IF), a strategy that reshapes nutrient availability and microbial dynamics. HFSD‑induced obese rats were treated for four weeks with SA leaf powder (300 mg/kg/day), IF, or both. Bioactive constituents of SA were characterized using LC‑HRMS, alongside systematic evaluation of physiological and metabolic parameters-including adiposity, morphometry, lipid profiles, insulin sensitivity markers, and gut-endocrine axis indicators. SA supplementation showed improvements across all parameters, surpassing those achieved with IF alone. Importantly, the combined intervention (SA+IF) yielded complementary benefits, notably enhancing GLUT4 expression, short‑chain fatty acid (SCFA) production, peptide YY (PYY) secretion, and reducing the Firmicutes/Bacteroidetes ratio. These findings highlight the complementary roles of SA and IF in metabolic regulation, providing experimental evidence for a potential dietary approach to mitigate obesity‑related dysfunction. - Source: PubMed
Fulyani FaizahWidayanti Iftitan SetyaBestari Salwa AlifaBatubara LusianaAriani R R Mahayu DewiRoosevelt D H CharlieFikri Muhammad IchsanulChandrawira GalenKusuma Rio Jati - Antipsychotic-associated metabolic toxicity remains one of the most persistent clinical problems in psychopharmacology. Clozapine and olanzapine are especially effective for psychosis but carry high liability for weight gain, dyslipidemia, insulin resistance, and type 2 diabetes. Current monitoring recommendations recognize this risk, yet they remain largely uniform across patients and do not incorporate ancestry-specific genetic risk or mechanistic drug-gene information. We performed a transcriptome-wide association study-informed drug-gene prioritization analysis to examine whether approved antipsychotic target genes overlap with genes whose genetically predicted expression is associated with type 2 diabetes. The analysis used ancestry-specific type 2 diabetes transcriptome-wide association study (TWAS) results derived from a multi-ancestry genome-wide association study (GWAS) and approved antipsychotic drug-gene interactions from the Drug-Gene Interaction Database (DGIdb). For each drug, target genes were matched to TWAS genes across six metabolic tissues, and a weighted risk score was calculated as the sum of the absolute TWAS z-score multiplied by the drug-gene interaction score for significant targets. Follow-up analyses decomposed signals into targets with positive and negative TWAS directions, operationally interpreted as aggravating and compensatory, while also examining curated metabolic axis genes including GLP1R, GIPR, PPARG, and SLC2A4. The analysis identified recurrent exploratory target-overlap signals for clozapine and olanzapine. Clozapine showed the most consistent cross-ancestry aggravating profile, with recurrent target overlap involving GLP1R and immune-related genes. Olanzapine showed strong mechanistic-axis overlap involving GLP1R, GIPR, and PPARG, although its simple TWAS directionality was often classified as compensatory. Trifluoperazine emerged as a notable candidate, with significant target enrichment in the European ancestry analysis and top ranking in the Hispanic analysis. Fluspirilene also met the combined enrichment false discovery rate threshold in the European ancestry analysis, although its clinical metabolic interpretation was less direct. Haloperidol decanoate showed a high burden driven partly by SLC2A4, but its directionality was frequently mixed or compensatory. These findings nominate the incretin axis as a plausible translational bridge between antipsychotic metabolic liability and existing interventions such as GLP-1 receptor agonists. They also identify a key methodological gap. Future models must incorporate the pharmacologic mode of action to distinguish receptor blockade from activation. Except for the enrichment-positive European ancestry findings for trifluoperazine and fluspirilene, the results are exploratory prioritization signals and do not establish drug-specific metabolic effects, causal mechanisms, or ancestry-specific treatment effects. Overall, this TWAS-informed analysis provides a hypothesis-generating framework for ancestry-aware metabolic monitoring and targeted validation studies. - Source: PubMed
Publication date: 2026/07/16
Cheung Ngo - Histone lactylation drives reparative macrophage responses after myocardial infarction. Our recent study identified exosomal CRNDE as a key mediator of exercise-induced cardioprotection. Given the role of CRNDE in glycolysis, the present study aimed to explore whether exercise-derived exosomes (exe-exo) alleviate myocardial injury by modulating inflammation through histone lactylation. - Source: PubMed
Publication date: 2026/07/13
Liu YanChen WujunYe QiaoyiDong YiDing Haifeng